A threshold lung volume for optimal mechanical effects on upper airway airflow dynamics: studies in an anesthetized rabbit model

2012 ◽  
Vol 112 (7) ◽  
pp. 1197-1205 ◽  
Author(s):  
Kristina Kairaitis ◽  
Manisha Verma ◽  
Jason Amatoury ◽  
John R. Wheatley ◽  
David P. White ◽  
...  
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Rabbit Model ◽  
Upper Airway ◽  
Flow Limitation ◽  
Volume Increase ◽  
Mechanical Effects ◽  
Pharyngeal Pressure ◽  
Volume Resistance ◽  
Spontaneously Breathing

Increasing lung volume improves upper airway airflow dynamics via passive mechanisms such as reducing upper airway extraluminal tissue pressures (ETP) and increasing longitudinal tension via tracheal displacement. We hypothesized a threshold lung volume for optimal mechanical effects on upper airway airflow dynamics. Seven supine, anesthetized, spontaneously breathing New Zealand White rabbits were studied. Extrathoracic pressure was altered, and lung volume change, airflow, pharyngeal pressure, ETP laterally (ETPlat) and anteriorly (ETPant), tracheal displacement, and sternohyoid muscle activity (EMG%max) monitored. Airflow dynamics were quantified via peak inspiratory airflow, flow limitation upper airway resistance, and conductance. Every 10-ml lung volume increase resulted in caudal tracheal displacement of 2.1 ± 0.4 mm (mean ± SE), decreased ETPlat by 0.7 ± 0.3 cmH2O, increased peak inspiratory airflow of 22.8 ± 2.6% baseline (all P < 0.02), and no significant change in ETPant or EMG%max. Flow limitation was present in most rabbits at baseline, and abolished 15.7 ± 10.5 ml above baseline. Every 10-ml lung volume decrease resulted in cranial tracheal displacement of 2.6 ± 0.4 mm, increased ETPant by 0.9 ± 0.2 cmH2O, ETPlat was unchanged, increased EMG%max of 11.1 ± 0.3%, and a reduction in peak inspiratory airflow of 10.8 ± 1.0%baseline (all P < 0.01). Lung volume, resistance, and conductance relationships were described by exponential functions. In conclusion, increasing lung volume displaced the trachea caudally, reduced ETP, abolished flow limitation, but had little effect on resistance or conductance, whereas decreasing lung volume resulted in cranial tracheal displacement, increased ETP and increased resistance, and reduced conductance, and flow limitation persisted despite increased muscle activity. We conclude that there is a threshold for lung volume influences on upper airway airflow dynamics.

Collapsibility of the Upper Airway during Anesthesia with Isoflurane

2002 ◽  
Vol 97 (4) ◽  
pp. 786-793 ◽  
Author(s):  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
David R. Hillman
Keyword(s):  
Lung Volume ◽  
Critical Pressure ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Flow Limitation ◽  
Anesthetic Depth ◽  
Volume Collapse ◽  
End Tidal ◽  
Spontaneously Breathing

Background The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. Methods To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. Results The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( &lt; 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( &lt; 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. Conclusions Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

scholarly journals Impaired Upper Airway Integrity by Residual Meeting Abstracts

2009 ◽  
Vol 110 (6) ◽  
pp. 1253-1260 ◽  
Author(s):  
Frank Herbstreit ◽  
Jürgen Peters ◽  
Matthias Eikermann
Keyword(s):  
Neuromuscular Blockade ◽  
Lung Volume ◽  
Upper Airway ◽  
Random Order ◽  
Compensatory Response ◽  
Residual Neuromuscular Blockade ◽  
Pharyngeal Pressure ◽  
Pressure Threshold ◽  
Airway Collapsibility ◽  
Closing Pressure

Background Residual neuromuscular blockade increases the risk to develop postoperative complications. The authors hypothesized that minimal neuromuscular blockade (train-of-four [TOF] ratio 0.5-1) increases upper airway collapsibility and impairs upper airway dilator muscle compensatory responses to negative pharyngeal pressure challenges. Methods Epiglottic and nasal mask pressures, genioglossus electromyogram, respiratory timing, and changes in lung volume were measured in awake healthy volunteers (n = 15) before, during (TOF = 0.5 and 0.8 [steady state]), and after recovery of TOF to unity from rocuronium-induced partial neuromuscular blockade. Passive upper airway closing pressure (negative pressure drops, random order, range +2 to -30 cm H2O) and pressure threshold for flow limitation were determined. Results Upper airway closing pressure increased (was less negative) significantly from baseline by 54 +/- 4.4% (means +/- SEM), 37 +/- 4.2%, and 16 +/- 4.1% at TOF ratios of 0.5, 0.8, and 1.0, respectively (P &lt; 0.01 vs. baseline for any level). Phasic genioglossus activity almost quadrupled in response to negative (-20 cm H2O) pharyngeal pressure at baseline, and this increase was significantly impaired by 57 +/- 44% and 32 +/- 6% at TOF ratios of 0.5 and 0.8, respectively (P &lt; 0.01 vs. baseline). End-expiratory lung volume, respiratory rate, and tidal volume did not change. Conclusion Minimal neuromuscular blockade markedly increases upper airway closing pressure, partly by impairing the genioglossus muscle compensatory response. Increased airway collapsibility despite unaffected values for resting ventilation may predispose patients to postoperative respiratory complications, particularly during airway challenges.

Thoracic influence on upper airway patency

1988 ◽  
Vol 65 (5) ◽  
pp. 2124-2131 ◽  
Author(s):  
W. B. Van de Graaff
Keyword(s):  
Muscle Activity ◽  
Upper Airway ◽  
Constant Flow ◽  
Airway Patency ◽  
Anesthetized Dogs ◽  
Measured Resistance ◽  
Flow Through ◽  
Phrenic Nerves ◽  
Tracheostomy Tubes ◽  
Spontaneously Breathing

Patency of the upper airway (UA) is usually considered to be maintained by the activity of muscles in the head and neck. These include cervical muscles that provide caudal traction on the UA. The thorax also applies caudal traction to the UA. To observe whether this thoracic traction can also improve UA patency, we measured resistance of the UA (RUA) during breathing in the presence and absence of UA muscle activity. Fifteen anesthetized dogs breathed through tracheostomy tubes. RUA was calculated from the pressure drop of a constant flow through the isolated UA. RUA decreased 31 +/- 5% (SEM) during inspiration. After hyperventilating seven of these dogs to apnea, we maximally stimulated the phrenic nerves to produce paced diaphragmatic breathing. Despite absence of UA muscle activity, RUA fell 51 +/- 11% during inspiration. Graded changes were produced by reduced stimulation. In six other dogs we denervated all UA muscles. RUA still fell 25 +/- 7% with inspiration in these spontaneously breathing animals. When all caudal ventrolateral cervical structures mechanically linking the thorax to the UA were severed, RUA increased and respiratory fluctuations ceased. These findings indicate that tonic and phasic forces generated by the thorax can improve UA patency. Inspiratory increases in UA patency cannot be attributed solely to activity of UA muscles.

Neostigmine/Glycopyrrolate Administered after Recovery from Neuromuscular Block Increases Upper Airway Collapsibility by Decreasing Genioglossus Muscle Activity in Response to Negative Pharyngeal Pressure

2010 ◽  
Vol 113 (6) ◽  
pp. 1280-1288 ◽  
Author(s):  
Frank Herbstreit ◽  
Daniela Zigrahn ◽  
Christof Ochterbeck ◽  
Jürgen Peters ◽  
Matthias Eikermann
Keyword(s):  
Neuromuscular Blockade ◽  
Lung Volume ◽  
Muscle Activation ◽  
Neuromuscular Block ◽  
Upper Airway ◽  
Acetylcholinesterase Inhibitors ◽  
Genioglossus Muscle ◽  
Pharyngeal Pressure ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Background Reversal of residual neuromuscular blockade by acetylcholinesterase inhibitors (e.g., neostigmine) improves respiratory function. However, neostigmine may also impair muscle strength. We hypothesized that neostigmine administered after recovery of the train-of-four (TOF) ratio impairs upper airway integrity and genioglossus muscle function. Methods We measured, in 10 healthy male volunteers, epiglottic and nasal mask pressures, genioglossus electromyogram, air flow, respiratory timing, and changes in lung volume before, during (TOF ratio: 0.5), and after recovery of the TOF ratio to unity, and after administration of neostigmine 0.03 mg/kg IV (with glycopyrrolate 0.0075 mg/kg). Upper airway critical closing pressure (Pcrit) was calculated from flow-limited breaths during random pharyngeal negative pressure challenges. Results Pcrit increased significantly after administration of neostigmine/glycopyrrolate compared with both TOF recovery (mean ± SD, by 27 ± 21%; P = 0.02) and baseline (by 38 ± 17%; P = 0.002). In parallel, phasic genioglossus activity evoked by negative pharyngeal pressure decreased (by 37 ± 29%, P = 0.005) compared with recovery, almost to a level observed at a TOF ratio of 0.5. Lung volume, respiratory timing, tidal volume, and minute ventilation remained unchanged after neostigmine/glycopyrrolate injection. Conclusion Neostigmine/glycopyrrolate, when administered after recovery from neuromuscular block, increases upper airway collapsibility and impairs genioglossus muscle activation in response to negative pharyngeal pressure. Reversal with acetylcholinesterase inhibitors may be undesirable in the absence of neuromuscular blockade.

Changes in end-expiratory lung volume during sleep in patients with occlusive apnea

1987 ◽  
Vol 63 (4) ◽  
pp. 1642-1647 ◽  
Author(s):  
R. M. Aronson ◽  
C. G. Alex ◽  
E. Onal ◽  
M. Lopata
Keyword(s):  
Lung Volume ◽  
Muscle Activity ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Esophageal Pressure ◽  
Inspiratory Pressure ◽  
Upper Airways ◽  
Airway Occlusion ◽  
Respiratory Inductive Plethysmography ◽  
Inductive Plethysmography

Eight patients with occlusive sleep apnea were monitored during non-rapid-eye-movement (NREM) sleep to study the factors that contribute to negative inspiratory pressure generation and thus upper airway occlusion. End-expiratory lung volume assessed by respiratory inductive plethysmography [sum of end-expiratory levels (SUM EEL)] increased early and decreased late during the ventilatory phases (P less than 0.0001, one-way analysis of variance). Inspiratory change in esophageal pressure (Pes) and peak inspiratory diaphragmatic and genioglossal electromyograms (EMGdi and EMGge) decreased while the inspiratory pressure generated for a given diaphragmatic activity (Pes/EMGdi) increased during the preapneic phase (P less than 0.0001, for all). Multiple regression analysis with Pes/EMGdi as the dependent variable (R2 = 0.90) indicated that both the changes in SUM EEL and EMGge significantly contributed to the model (P less than 0.008 and 0.004, respectively). These results indicate that end-expiratory lung volume fluctuates during NREM sleep in patients with occlusive apnea and suggest that these changes along with the changes in upper airway muscle activity contribute to the generation of negative inspiratory pressure, leading to the passive collapse of the upper airways.

scholarly journals Modulation of laryngeal and respiratory pump muscle activities with upper airway pressure and flow

2001 ◽  
Vol 91 (2) ◽  
pp. 897-904 ◽  
Author(s):  
M. H. Stella ◽  
S. J. England
Keyword(s):  
Negative Pressure ◽  
Muscle Activity ◽  
Upper Airway ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Emg Activity ◽  
Posterior Cricoarytenoid ◽  
Spontaneously Breathing ◽  
Respiratory Muscle Activity ◽  
Stimulation Of

The hypothesis that upper airway (UA) pressure and flow modulate respiratory muscle activity in a respiratory phase-specific fashion was assessed in anesthetized, tracheotomized, spontaneously breathing piglets. We generated negative pressure and inspiratory flow in phase with tracheal inspiration or positive pressure and expiratory flow in phase with tracheal expiration in the isolated UA. Stimulation of UA negative pressure receptors with body temperature air resulted in a 10–15% enhancement of phasic moving-time-averaged posterior cricoarytenoid electromyographic (EMG) activity above tonic levels obtained without pressure and flow in the UA (baseline). Stimulation of UA positive pressure receptors increased phasic moving-time-averaged thyroarytenoid EMG activity above tonic levels by 45% from baseline. The same enhancement of posterior cricoarytenoid or thyroarytenoid EMG activity was observed with the addition of flow receptor stimulation with room temperature air. Tidal volume and diaphragmatic and abdominal muscle activity were unaffected by UA flow and/or pressure, whereas respiratory timing was minimally affected. We conclude that laryngeal afferents, mainly from pressure receptors, are important in modulating the respiratory activity of laryngeal muscles.

Collapsibility of the Upper Airway at Different Concentrations of Propofol Anesthesia

2005 ◽  
Vol 103 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Peter R. Eastwood ◽  
Peter R. Platt ◽  
Kelly Shepherd ◽  
Kathy Maddison ◽  
David R. Hillman
Keyword(s):  
Upper Airway ◽  
Inspiratory Flow ◽  
Electromyographic Activity ◽  
Flow Limitation ◽  
Genioglossus Muscle ◽  
Airway Collapsibility ◽  
Effect Site Concentration ◽  
Intramuscular Electrodes ◽  
Upper Airway Collapsibility ◽  
Spontaneously Breathing

Background This study investigated the effect of varying concentrations of propofol on upper airway collapsibility and the mechanisms responsible for it. Methods Upper airway collapsibility was determined from pressure-flow relations at three concentrations of propofol anesthesia (effect site concentration = 2.5, 4.0, and 6.0 mug/ml) in 12 subjects spontaneously breathing on continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (maintenance pressure = 12 +/- 1 cm H2O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. Electromyographic activity of the genioglossus muscle (EMGgg) was obtained via intramuscular electrodes in 8 subjects. Results With increasing depth of anesthesia, (1) critical closing pressure progressively increased (-0.3 +/- 3.5, 0.5 +/- 3.7, and 1.4 +/- 3.5 cm H2O at propofol concentrations of 2.5, 4.0, and 6.0 microg/ml respectively; P &lt; 0.05 between each level), indicating a more collapsible upper airway; (2) inspiratory flow at the maintenance pressure significantly decreased; and (3) respiration-related phasic changes in EMGgg at the maintenance pressure decreased from 7.3 +/- 9.9% of maximum at 2.5 microg/ml to 0.8 +/- 0.5% of maximum at 6.0 microg/ml, whereas tonic EMGgg was unchanged. Relative to the levels of phasic and tonic EMGgg at the maintenance pressure immediately before a decrease in mask pressure, tonic activity tended to increase over the course of five flow-limited breaths at a propofol concentration of 2.5 microg/ml but not at propofol concentrations of 4.0 and 6.0 microg/ml, whereas phasic EMGgg was unchanged. Conclusions Increasing depth of propofol anesthesia is associated with increased collapsibility of the upper airway. This was associated with profound inhibition of genioglossus muscle activity. This dose-related inhibition seems to be the combined result of depression of central respiratory output to upper airway dilator muscles and of upper airway reflexes.

Effect of negative expiratory pressure on respiratory system flow resistance in awake snorers and nonsnorers

1999 ◽  
Vol 87 (3) ◽  
pp. 969-976 ◽  
Author(s):  
Claudio Tantucci ◽  
Alexandre Duguet ◽  
Anna Ferretti ◽  
Selma Mehiri ◽  
Isabelle Arnulf ◽  
...  
Keyword(s):  
Respiratory System ◽  
Supine Position ◽  
Flow Resistance ◽  
Upper Airway ◽  
Flow Limitation ◽  
Expiratory Flow Limitation ◽  
Upper Airways ◽  
Flow Interruption ◽  
Expiratory Flow ◽  
Spontaneously Breathing

In spontaneously breathing subjects, intrathoracic expiratory flow limitation can be detected by applying a negative expiratory pressure (NEP) at the mouth during tidal expiration. To assess whether NEP might increase upper airway resistance per se, the interrupter resistance of the respiratory system (Rint,rs) was computed with and without NEP by using the flow interruption technique in 12 awake healthy subjects, 6 nonsnorers (NS), and 6 nonapneic snorers (S). Expiratory flow (V˙) and Rint,rs were measured under control conditions with V˙ increased voluntarily and during random application of brief (0.2-s) NEP pulses from −1 to −7 cmH2O, in both the seated and supine position. In NS, Rint,rs with spontaneous increase inV˙ and with NEP was similar [3.10 ± 0.19 and 3.30 ± 0.18 cmH2O ⋅ l−1 ⋅ s at spontaneous V˙ of 1.0 ± 0.01 l/s and atV˙ of 1.1 ± 0.07 l/s with NEP (−5 cmH2O), respectively]. In S, a marked increase in Rint,rs was found at all levels of NEP ( P < 0.05). Rint,rs was 3.50 ± 0.44 and 8.97 ± 3.16 cmH2O ⋅ l−1 ⋅ s at spontaneous V˙ of 0.81 ± 0.02 l/s and atV˙ of 0.80 ± 0.17 l/s with NEP (−5 cmH2O), respectively ( P < 0.05). With NEP, Rint,rs was markedly higher in S than in NS both seated ( F = 8.77; P < 0.01) and supine ( F = 9.43; P < 0.01). In S,V˙ increased much less with NEP than in NS and was sometimes lower than without NEP, especially in the supine position. This study indicates that during wakefulness nonapneic S have more collapsible upper airways than do NS, as reflected by the marked increase in Rint,rs with NEP. The latter leads occasionally to an actual decrease in V˙ such as to invalidate the NEP method for detection of intrathoracic expiratory flow limitation.

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